Transcript Skin lesions I

Monday
AM
report
11-23-09
CC:
Weakness, myalgias,
arthralgias and fever
Bring it on!
HPI
ROS
Chemistry
Immunology
Meds/Allergies
FH/SH
LFTs
Coags
PE I
Heme
Microbiology
PE II
Problem list
Urinalysis
Molecular
Microbiology
Endocrine
Toxicology
Pathology
US
Chest X-ray
Abdomen X-ray
Extremities X-ray
CT head
CT chest
CT abdomen
CT extrem/bone
MRI head
MRI chest
MRI abdomen
MRI
extrem/bone
EKG
TTE
TEE
PVL
Lecture
HPI
HPI: This is a 54 yo caucasian male who was transferred from Maria Parham ED for a several
day history of generalized weakness, muscle aches with associated subjective fevers (101 F)
that started 5 days ago with a sore throat. He was in his usual state of health who reports that
approximately 3 weeks ago he hurt his back while lifting a heavy television. As a result of this
injury, he began to experience sharp pains that would go down his left leg. He was seen in the
Maria Parham ED, who obtained a MRI spine that revealed a "pinched nerve" from a possible
slipped disc. He was referred to an orthopedist in Raleigh, who prescribed cyclobenzaprine
and physical therapy with good response. After that he developed a fever 5 days ago followed
closely by myalgias, nausea/vomiting, headaches that converted to migraines, and general
weakness. He presented to Maria Parham again, who diagnosed him with the flu, gave fluid
resuscitation, and sent him home. However, his symptoms continued to a point where he
could no longer walk, and re-presented at Maria Parham ED for evaluation. At that time, he
was noted by the physician there to have bilateral lower extremity weakness and diminished
reflexes. Out of concern for possible acute inflammatory demyelinating polyneuropathy
(Guillian-Barre syndrome) he was transferred to UNC. He also developed swelling and
tenderness of the right knee on Sunday. He developed a red patchy rash on his elbows 3
weeks ago. He also developed purple papules on palms and soles that have worsened over
the course of
the day.
Back
ROS
GENERAL: +appetite loss, +chills, no nightsweats, mild weight loss due to appetite loss
HEENT: +HA, +Nausea/vomiting, + sore throat, no vision changes
CHEST: no chest pain
LUNGS: no SOB, no cough, no hemoptysis
ABDOMEN: no abdominal pain, no diarrhea, no blood in stools
GU: no urinary symptoms, no discharge
MSK: generalized myalgias and arthralgias, back pain
SKIN: + jaundice, bilateral elbows with red patchy rash with a few pustules, petechial rash on
right chest medial to mid axillary line, purple pustules present on soles of hands and feet.
Neuro/Psych: 3xoriented, anxious, general weakness
Back
PMH - Meds/allergies - FH/SH
PMH:
HTN
HLD
Gilbert's Syndrome
Osteoarthritis in Neck
Low back pain since 3 weeks with radicular, pinched nerve at L3-L4 from lifting injury
PSH:
Appendectomy at age 12
Kidney stones lithotripsy x 5
L inguinal hernia repair 2005
Crown lengthening procedure about 1 month to 6 weeks ago and a root canal a few weeks prior to that
CURRENT MEDS:
HCTZ 25mg daily
Simvastatin 40 mg daily
Skelaxin (metaxalone) 400mg bid (muscle relaxant)
ASA 81 mg
Etodolac 400mg BID
Vitamins E and C
Allergies:
NKDA
SH
No tobacco, No ETOH, No history of IV drug use, No history of sexually transmitted disease. Currently
working as support analyst at Lab Core in Burlington. Lives in Henderson with wife. 2 Children
FH
3. Cousin had toe fungus (JUST kidding!). Noncontributory!
Back
PE
T 98.7
RR 22
HR 115
BP 116/68
Sa O2 96 % on RA
PE
General: Pt. in acute distress, diaphoretic
HEENT: Mouth dry, no palatal petechia or aphtae, yellow sclera, no JVD
Heme: no LAD
CV: S1, S2, rapid regular, no murmur, no rub, no gallop
Lungs: CTAB, no wheezes
Abdomen: soft, nontender, nondistended, +hemorrhoids
Skin: Purpule pustules present on soles of hands and feet, petechial rash on right
chest medial to mid axillary line, + jaundice, bilateral elbows with red patchy rash
with a few pustules.
GU: no discharge
MSK: Decreased strength due to pain.
Extremities: R knee effusion, no erythema, no warmth, pulses 2+ throughout
Neuro: AAOx 3, no focal, DTRs 2+ bilaterally, sensation intact, Babinski negative,
CNs 2-12 grossly intact
Back
Skin lesions I
Next
Skin lesions II
Next
Skin lesions III
Back
Problem list
Weakness
Myalgias
Arthralgias (+ right knee swelling)
Subjective fevers
Tachycardia
Low O2 sats
Jaundice
Headaches
Nausea/vomiting
Dehydration
Pain
Skin lesions (elbow, palms, soles, petechia on chest)
Back
Chemistry
Sodium 140
Potassium 3.9
Chloride 104
CO2 30
BUN 39
Creatinine 1.54 (GFR 45) Stage 3
Glucose 115
Calcium 8
Magnesium 1.8
Phosphorus 4
CK 134
CK-MB 3.6
Troponin 0.48 !!!
Protein 5.3
Albumin 2.7
LD 687
Back
LFTs
Bilirubin 4.2 (direct 1.2)
AST 234
ALT 435
AP 113
GGT 65
Back
Coags
INR 1.5
PTT 33.2
Back
Heme
CBC 9.7 (peak 4days later 17.2)
Platelets 73
H&H 12.1/34.5
Back
Urinalysis
Urine sodium <5
FeNa 0!
UA:
WBC 6
LE+
Prot 1+
RBC 17
Back
Endocrine
TSH 3.53
Cortisol normal
Back
Immunology
CRP >45
HIV negative
Hepatitis B,C negative
ANA negative
ANCA negative
RF negative
Glomerular basement membrane -Ab negative
Back
Microbiology
BC (3/3):
MRSA (community acquired)
Took 3 days to clear BCs
UC (MRSA)
Vitrous fluid negative 2+PMN
Knee + L3/4 disk negative (50000 cells 95% neutrophils)
Back
Molecular
Microbiology
Toxoplasma negative
EBV negative
CMV negative
VZV negative
HSV negative
Chlamydia negative
GC negative
Back
Toxicology
Back
Pathology
Diagnosis:
Synovium, right knee, biopsy
- Acute and chronic synovitis.
Back
EKG
Sinustachycardia
Back
TTE
EF 55%
No vegetations
Back
TEE
No vegetations
Back
Renal US
No hydronephrosis or nephrolithiasis.
Back
PVL
No DVT
Back
Chest x-ray
1. Diffuse patchy opacities identified bilaterally consistent
with mild pulmonary edema versus infection.
2. Question small bilateral pleural effusions versus
overlying soft tissue.
Back
CT head
No acute intracranial abnormality is
identified.
Back
MRI spine
Cervical spine:
IMPRESSION: Multilevel degenerative disk disease. No
abnormal cord signal or enhancement.
Thoracic spine:
IMPRESSION: Unremarkable pre-and postcontrast MRI of
the thoracic spine.
Lumbar spine:
IMPRESSION: Increased STIR signal and enhancement
involving theposterior elements from L3 through L5 as
well as the dorsalepidural space at this region. This could
be related to inflammatory changes from recent lumbar
puncture versus aninfectious process. No drainable fluid
collections or masseffect in the spinal canal is present.
Back
MRI head
Next
MRI head
Back
CT chest/abdomen/pelvis
IMPRESSION:
1. Distal position of right PICC line as above.
2. Splenic and renal hypodensities are indeterminant given
size.
3. Trace pelvic fluid. Gas within bladder may be secondary
to Foley placement.
4. Mild splenomegaly.
Back
Endocarditis
• Infectious Endocarditis (IE): an infection of
the heart’s endocardial surface
• Classified into four groups:
– Native Valve IE
– Prosthetic Valve IE
– Intravenous drug abuse (IVDA) IE
– Nosocomial IE
Further Classification
• Acute
– Affects normal heart
valves
– Rapidly destructive
– Metastatic foci
– If not treated, usually
fatal within 6 weeks
Organisms:
Staphylococcus aureus,
Streptococcus pyogenes,
Streptococcus pneumoniae
• Subacute
– Often affects damaged
heart valves
– Indolent nature
– If not treated, usually
fatal by one year
Organisms:
Streptococcus viridans
Enterococcus
Infective Endocarditis
• Gram negative organisms
– P. aeruginosa most common
– HACEK - slow growing, fastidious organisms that
may need 3 weeks to grow out of culture
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Haemophilus sp.
Actinobacillus
Cardiobacterium
Eikenella
Kingella
Infective Endocarditis
• Case rate may vary between 2-3 cases /100,000 to
as high as 15-30/100,000 depending on incidence of
i.v. drug abuse and age of the population
– 55-75% of patients with native valve endocarditis (NVE)
have underlying valve abnormalities
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•
MVP
Rheumatic
Congenital
ASH or:
i.v. drug abuse
Infective Endocarditis
• Adult population
– Rheumatic Heart Disease
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20 – 25% of cases of IE in 1970’s & 80’s
7 – 18% of cases in recent reported series
Mitral site more common in women
Aortic site more common in men
– Congenital Heart Disease
• 10 – 20% of cases in young adults
• 8% of cases in older adults
• PDA, VSD, bicuspid aortic valve (esp. in men>60)
Infective Endocarditis
• Intravenous Drug Abuse
– Risk is 2 – 5% per pt./year
– Tendency to involve right-sided valves
• Distribution in clinical series
– 46 – 78% tricuspid
– 24 – 32% mitral
– 8 – 19% aortic
– Underlying valve normal in 75 – 93%
– S. aureus predominant organism (>50%, 60-70%
of tricuspid cases)
Clinical Features I
• Interval between index bacteremia & onset
of sx’s usually < 2 weeks
• May be substantially longer in early PVE
• Fever most common sign
• May be absent in elderly/debilitated pt.
• Murmur present in 80 – 85%
• Generally indication of underlying lesion
• Frequently absent in tricuspid IE
• Changing murmur
Clinical Features II
• Acute
– High grade fever and
chills
– SOB
– Arthralgias/
myalgias
– Abdominal pain
– Pleuritic chest pain
– Back pain
• Subacute
– Low grade fever
– Anorexia
– Weight loss
– Fatigue
– Arthralgias/
myalgias
– Abdominal pain
– N/V
Petechiae
1. Nonspecific
2. Often located on extremities
or mucous membranes
Janeway Lesions
Janeway Lesions
1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles
Splinter Hemorrhage
Splinter Hemorrhages
1. Nonspecific
2. Nonblanching
3. Linear reddish-brown lesions found under the nail bed
4. Usually do NOT extend the entire length of the nail
Osler’s Nodes
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common in subacute IE
Subconjunctival Hemorrhages
Roth’s Spots
Complications
• Four etiologies
– Embolic
– Local spread of infection
– Metastatic spread of infection
– Formation of immune complexes –
glomerulonephritis and arthritis
Embolic Complications
• Occur in up to 40% of patients with IE
• Stroke
• Myocardial Infarction
– Fragments of valvular vegetation or vegetationinduced stenosis of coronary ostia
• Ischemic limbs
• Hypoxia from pulmonary emboli
• Abdominal pain (splenic or renal infarction)
Septic Pulmonary Emboli
Local Spread of Infection
• Heart failure
– Extensive valvular damage
• Paravalvular abscess (30-40%)
– Most common in aortic valve, IVDA, and S. aureus
– May extend into adjacent conduction tissue causing
arrythmias
– Higher rates of embolization and mortality
• Pericarditis
• Fistulous intracardiac connections
Modified Duke Criteria
2 Major OR 1 Major + 3 Minor OR 5 Minor.
Major (microbiology):
a) typical organisms x 2 blood cultures (e.g., Strep viridans, S. bovis, HACEK, S.
aureus, or enterococcus) with no primary source,
b) persistent bacteremia (>12 hours),
c) 3/3 or 3/4 positive blood cultures.
Major (valve):
a) echo w/ vegetation
b) b) new valve regurgitation.
Minor:
a) predisposing cardiac condition or IDU,
b) fever > 38°C (100.4°F)
c) vascular phenomenon (arterial emboli, mycotic aneurysm, intracerebral bleed,
conjunctival hemorrhage, Janeway lesions)
d) immune phenomenon (glomerulonephritis, Osler nodes, Roth spots, positive
rheumatoid factor)
e) positive blood culture not meeting above criteria and
f) echo--abnl but not diagnostic.
Antibiotic Therapy
• Effective antimicrobial treatment should lead
to defervescence within 7 – 10 days
•Empiric, acute endocarditis:
[nafcillin or oxacillin 2g IV q4h + gentamicin or tobramycin 1mg/kg IV q8h]
OR [vancomycin 15mg/kg IV q12h + gentamicin 1mg/kg IV q8h].
•Empiric, subacute endocarditis:
[ampicillin/sulbactam 3g IV q 6h + gentamicin or tobramycin 1mg/kg IV
q8h] OR [vancomycin 15mg/kg q12h + [ceftriaxone 2g IV q12hOR
gentamicin/tobramycin 1 mg/kg IV q8h].
Prophylactic Therapy
Bacteremia Risk Related to Dental Procedures
Estimated cumulative exposure of 5370 minutes of bacteremia/
month related to chewing food and oral hygiene measure Vs. 6-30
minutes of bacteremia associated with single tooth extraction
(Guntheroth 1984).
Tooth brushing twice daily for 1 year has estimated IE risk 154,000
times greater than single tooth extraction (Roberts, 1999).
Cumulative exposure to bacteremia over 1 year may be as high as
5.6 million times greater than that from a single tooth extraction
(Roberts, 1999)..
Cardiac Conditions for which IE Prophylaxis
Recommended for Dental Procedures
• Prosthetic Cardiac Valve
• Previous Infective Endocarditis
• Congenital Heart Disease (CHD)
• Unrepaired Cyanotic CHD, Including Palliative Shunts and Conduits
• Completely Repaired CHD with Prosthetic Material or Device, whether by
Surgery or by Catheter Intervention, during the first 6 months after the procedure
• Repaired CHD with Residual Defects at the Site or Adjacent to the Site of a
Prosthetic Patch or Prosthetic Device (which Inhibit Endothelialization)
• Cardiac Transplant Recipients who Develop Valvulopathy
• All dental procedures that involve manipulation of gingival tissue or the
periapical region of teeth or perforation of the oral mucosa.
Endocarditis Prophylaxis NOT Recommended:
• “Probably Innocent Murmur” never evaluated by cardiologist but
getting SBE prophylaxis “just in case.”
• Genitourinary or Gastrointestinal Tract Procedures.
Wilson W, Taubert KA, Gerwitz M, et al. Circulation. 2007;115.
IE Prophylaxis Dosing for Dental Procedure
• Oral: Administer 30-60 minutes prior to procedure.
• Amoxicillin*: 50 mg/kg (maximum 2 grams)
• Clindamycin: 20 mg/kg (maximum 600 milligrams)
• Cephalexin or equivalent 1st/2nd Generation Cephalosporin: 50
mg/kg (max. 2 grams)
• Azithromycin or Clarithromycin: 15 mg/kg (max. 500 mg)
• IVor IM: Administer 30-60 minutes prior to procedure.
• Ampicillin*: 50 mg/kg (maximum 2 grams)
• Cephazolin or Ceftriaxone*: 50 mg/kg (maximum 1 gram)
• Clindamycin: 20 mg/kg (maximum 600 mg)
*First choice unless allergic.
Wilson W, Taubert KA, Gerwitz M, et al. Circulation. 2007;115.
Thank you
Infective Endocarditis
• Pathology
– NVE infection is largely confined to leaflets
– PVE infection commonly extends beyond valve
ring into annulus/periannular tissue
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•
•
Ring abscesses
Septal abscesses
Fistulae
Prosthetic dehiscence
– Invasive infection more common in aortic position
and if onset is early
Infective Endocarditis
• Pathogenesis
Endothelial damage
Platelet-fibrin thrombi
Microorganism adherence
Pathophysiology
1. Turbulent blood flow disrupts the
endocardium making it “sticky”
2. Bacteremia delivers the organisms to the
endocardial surface
3. Adherence of the organisms to the
endocardial surface
4. Eventual invasion of the valvular leaflets
Endocarditis Prophylaxis NOT Recommended:
Negligible-risk Category
(No greater risk than the general population)
􀂄 Isolated secundum atrial septal defect
􀂄 Surgical repair of atrial septal defect, ventricular septal
defect, or patent ductus arteriosus (without residua
beyond 6 mo)
􀂄 Previous coronary artery bypass graft surgery
􀂄 Mitral valve prolapse without valvar regurgitation
􀂄 Physiologic, functional, or innocent heart murmurs
􀂄 Previous Kawasaki disease without valvar dysfunction
􀂄 Previous rheumatic fever without valvar dysfunction
􀂄 Cardiac pacemakers (intravascular and epicardial) and
implanted defibrillators
American Heart Association SBE Guidelines- JAMA 1997;277:1794
Infectious Bacterial Endocarditis
Prophylaxis No Longer Recommended
for the Following Conditions
􀂄 Ventricular Septal Defect
􀂄 Ostium Primum Atrial Septal Defect
􀂄 Pulmonary Stenosis
􀂄 Aortic Stenosis/Insufficiency
􀂄 Mitral Valve Prolapse with Valve Regurgitation
􀂄 Patent Ductus Arteriosus
􀂄 Coarctation of Aorta
􀂄 Rheumatic Heart Disease
􀂄 Hypertrophic Cardiomyopathy